dc.creator | Torres-Fuentes, Cristina | es |
dc.creator | Pastor Cavada, Elena | es |
dc.creator | Cano, Rafael | es |
dc.creator | Kandil, Dalia | es |
dc.creator | Shanahan, Rachel | es |
dc.creator | Juan Rodríguez, Rocío | es |
dc.creator | Shaban, Hamdy | es |
dc.creator | McGlacken, Gerard P. | es |
dc.creator | Schellekens, Harriët | es |
dc.date.accessioned | 2018-08-06T07:23:56Z | |
dc.date.available | 2018-08-06T07:23:56Z | |
dc.date.issued | 2018 | |
dc.identifier.citation | Torres-Fuentes, C., Pastor Cavada, E., Cano, R., Kandil, D., Shanahan, R., Juan Rodríguez, R.,...,Schellekens, H. (2018). Quinolones modulate ghrelin receptor signaling: potential for a novel small molecule scaffold in the treatment of cachexia. International Journal o f Molecular Sciences, 19, 1605. | |
dc.identifier.issn | 1422-0067 | es |
dc.identifier.uri | https://hdl.handle.net/11441/77834 | |
dc.description.abstract | Cachexia is a metabolic wasting disorder characterized by progressive weight loss,
muscle atrophy, fatigue, weakness, and appetite loss. Cachexia is associated with almost all major
chronic illnesses including cancer, heart failure, obstructive pulmonary disease, and kidney disease
and significantly impedes treatment outcome and therapy tolerance, reducing physical function and
increasing mortality. Current cachexia treatments are limited and new pharmacological strategies are
needed. Agonists for the growth hormone secretagogue (GHS-R1a), or ghrelin receptor, prospectively
regulate the central regulation of appetite and growth hormone secretion, and therefore have
tremendous potential as cachexia therapeutics. Non-peptide GHS-R1a agonists are of particular interest,
especially given the high gastrointestinal degradation of peptide-based structures, including that of
the endogenous ligand, ghrelin, which has a half-life of only 30 min. However, few compounds have
been reported in the literature as non-peptide GHS-R1a agonists. In this paper, we investigate the
in vitro potential of quinolone compounds to modulate the GHS-R1a in both transfected human cells
and mouse hypothalamic cells. These chemically synthesized compounds demonstrate a promising
potential as GHS-R1a agonists, shown by an increased intracellular calcium influx. Further studies are
now warranted to substantiate and exploit the potential of these novel quinolone-based compounds as
orexigenic therapeutics in conditions of cachexia and other metabolic and eating disorders. | es |
dc.description.sponsorship | Irish Research Council for Science and Technology (IRCSET) | es |
dc.description.sponsorship | Science Foundation Ireland (SFI/12/IP/1315) | es |
dc.description.sponsorship | Science Foundation Ireland (SFI/12/RC/2275) | es |
dc.description.sponsorship | Science Foundation Ireland (SFI/12/RC/2273) | es |
dc.description.sponsorship | Universidad de Sevilla | es |
dc.format | application/pdf | es |
dc.language.iso | eng | es |
dc.publisher | MDPI | es |
dc.relation.ispartof | International Journal o f Molecular Sciences, 19, 1605. | |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject | Ghrelin | es |
dc.subject | Quinolones | es |
dc.subject | Cachexia | es |
dc.subject | GHS-R1a | es |
dc.title | Quinolones modulate ghrelin receptor signaling: potential for a novel small molecule scaffold in the treatment of cachexia | es |
dc.type | info:eu-repo/semantics/article | es |
dcterms.identifier | https://ror.org/03yxnpp24 | |
dc.type.version | info:eu-repo/semantics/publishedVersion | es |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | es |
dc.contributor.affiliation | Universidad de Sevilla. Departamento de Biología Vegetal y Ecología | es |
dc.relation.projectID | SFI/12/IP/1315 | es |
dc.relation.projectID | SFI/12/RC/2275 | es |
dc.relation.projectID | SFI/12/RC/2273 | es |
dc.identifier.doi | 10.3390/ijms19061605 | es |
idus.format.extent | 15 | es |
dc.journaltitle | International Journal o f Molecular Sciences | es |
dc.publication.volumen | 19 | es |
dc.publication.initialPage | 1605 | es |